International Journal of Pediatric Otorhinolaryngology Extra
Volume 2, Issue 1 , Pages 31-33, March 2007

Facial paralysis in an infant with infectious mononucleosis

Pamukkale University, Faculty of Medicine, Department of Pediatrics, 20100 Denizli, Turkey

Received 6 July 2006; received in revised form 22 November 2006; accepted 23 November 2006.

Article Outline

Summary 

Infectious mononucleosis is caused by Epstein–Barr virus, and is rarely seen in infancy. Clinical findings include exudative tonsillitis, generalized or cervical lymphadenopathy, and hepatosplenomegaly. Many complications can arise, but these rarely include facial paralysis. We reported a 19-month-old patient who developed facial paralysis secondary to infectious mononucleosis.

Keywords: Epstein–Barr virus infection, Facial paralysis, Childhood

 

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1. Introduction 

Infectious mononucleosis is a clinical syndrome caused by Epstein–Barr virus (EBV) [1]. In developing countries, asymptomatic infection and seroconversion are frequent in early childhood [1], [2], [3]. In children with symptomatic EBV infection, fatigue, fever, exudative tonsillitis, generalized or cervical lymphadenopathy and hepatosplenomegaly are seen [1], [4]. Sometimes airway obstruction, myocarditis, splenic abscess and rupture, thrombocytopenia or neutropenia can be seen. Neurological complications include seizures, meningoencephalitis, transverse myelitis, Guillain–Barré syndrome, autonomic neuropathy and rarely facial paralysis [1], [2], [4], [5]. Here, we present a patient who developed unilateral facial paralysis during infectious mononucleosis.

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2. Case report 

A 19-month-old boy was brought to our hospital with the complaints that the left side of his mouth was drawn and that he was unable to close his right eye. According to the history obtained from the family, both sides of the child's anterior neck had become increasingly swollen during the past two days, and the facial symptoms had appeared on the day before the hospital visit.

On physical examination, the child was pale; his tonsils were hyperemic and hypertrophied and covered by a dirty-yellow membrane. There were two lymph nodes measuring 3cm×2cm and 2cm×2cm, on the left anterior cervical region while on the right there was one measuring 3cm×3cm. The patient was unable to close his right eye. The right nasolabial sulcus was absent, and the mouth was drawn to the left side in the patient (Fig. 1). According to House Brackmann Classification, the facial nerve paralysis level was Grade VI at the time of presentation.

Laboratory examinations revealed the following: hemoglobin 7.1g/dL, hematocrit 25.3%, WBC 14,400/mm3, RBC 4.12M/μL, platelets 385,000/mm3, MCV 52fL, MCH 29.2pg, MCHC 32.4g/dL and RDW 19.6%. The peripheral blood smear showed 31% monocytes, 6% Downey cells, 35% lymphocytes and 28% polymorphonuclear leukocytes and hypochromia, microcytosis, anisocytosis and poikilocytosis. Ferritin level was <3ng/dL. The test of heterophile antibody was negative but was positive for EBV-VCA Ig M. With these findings, the patient was diagnosed as infectious mononucleosis with facial paralysis on the right side. Oral prednisolone therapy was started at a dose of 2mg/kg/day. Artificial tears and closure of the eye at night were recommended. For the iron deficiency anemia ferrous iron therapy was started.

In the first week of treatment, the lymph nodes regressed but there was minimal correction of the patient's inability to close his right eye. The patient's peripheral blood smear showed 20% monocytes, 4% Downey cells, 30% lymphocytes and 46% polymorphonuclear leukocytes.

In the second week of treatment, the patient still could not close his right eye. On the peripheral blood smear, Downey cells were not seen and monocytes had decreased to 4%. In follow up the facial nerve paralysis level was Grade VI. We observed no recovery for prednisolone therapy. So the treatment was tapered and stopped.

In the third week, the patient's facial paralysis had not markedly improved and methyl prednisolone was given orally in a single dose of 30mg/kg. Cranial MRI taken in the end of first month was normal. By the third month after the initial visit, the facial palsy had completely resolved. The facial nerve paralysis level was Grade I. Laboratory values at this time were as follows: hemoglobin 12.4g/dL, hematocrit 38.4%, WBC 8400/mm3, RBC 4.95M/μL, platelets 320,000/mm3, MCV 71fL, MCH 31.4pg, MCHC 33.5g/dL, RDW 27.3% and ferritin 20ng/dL. The patient tested negative for EBV-VCA Ig M and positive for EBV-VCA Ig G. Iron therapy was continued for 1 month further.

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3. Discussion 

EBV is a lymphotrophic, double-stranded DNA virus [6]. It is transmitted via saliva and multiplies in oropharyngeal epithelium and in the parotid gland. It inhabits the lymphoreticular system, liver, spleen and B lymphocytes in the peripheral blood. After 4–8 weeks of incubation, clinical signs and symptoms emerge [5], [6]. Diagnosis is based on physical examination, peripheral blood smear findings and EBV-related serologic tests [6].

Neurological complications of infectious mononucleosis are not frequent (0.3–7.3%) [7], [8]. Infectious mononucleosis related facial paralysis is quite rare. Its pathogenesis is not completely known but is thought to involve the virus's direct entry into neurons and the resulting immune response of the central nervous system [9]. Facial paralysis related to infectious mononucleosis was first described by Gsell in 1937 [10]. In a study of 113 children with infectious mononucleosis, Sumaya and Ench found neurological complications in 3.5% and facial paralysis in 0.9% [4]. Terada et al. have recently reported EBV-related bilateral facial paralysis [11]. The incidence of bilateral facial nerve palsy among facial nerve palsy patients has ranged from 0.3 to 2% [12]. Table 1 summarizes the cases of EBV-related facial paralysis that have been reported in literature. As seen in Table 1, all nine patients were less than 2 years old. Our patient's age was 19 months. EBV-related facial paralysis is probably seen under 2 years of age more frequently.

Table 1. Reported cases of EBV-related facial paralysis in literature
StudyAge (months)GenderReported yearReference no.
Jounouchi et al.12Female1978[13]
Esumi et al.8Male1984[14]
Andersson and Sterner16Female1985[3]
Wilson and Grant16Female1997[2]
Yanagihara et al.24Male2000[15]
Schaller et al.15Male2000[16]
Mori et al.17Female2002[9]
Terada et al.14Female2003[11]

Facial paralysis in children has been reported to heal slowly, with 90% of function usually returning within 6 months [17], [18]. The use of corticosteroids to reduce neural edema and quicken recovery is controversial, but some studies recommend this therapy [19], [20], [21]. We applied corticosteroid therapy in the patient reported here. We first gave prednisolone for 3 weeks at the standard dose (2mg/kg/day). When the response to this was insufficient we applied a single megadose of methyl prednisolone (30mg/kg). By the third month of follow-up, the patient had recovered but we do not attribute this to the steroid.

In conclusion, facial paralysis is a rarely seen complication of EBV infection. It is most frequently seen in infants, and tends to resolve spontaneously in 3–6 months.

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References 

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PII: S1871-4048(06)00104-3

doi:10.1016/j.pedex.2006.11.005

International Journal of Pediatric Otorhinolaryngology Extra
Volume 2, Issue 1 , Pages 31-33, March 2007

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